Current advances in the understanding of the complex molecular mechanisms of BE development, which came from experimental models of BE, include overexpression of cyclooxygenase-2 (COX-2) [15,16], epidermal growth factor (EGF) [17,18,19], or mitogen-activated protein kinase (MAPK) and the protein kinase phosphorylation (PI3K) pathways [20,21], as well as increased secretion of gastrin due to achlorhydria as a complication of prolonged proton pomp inhibitors (PPI) therapy [22]. This evidence concerns the gene WNK2 and Barrett esophagus.